基于TLR4/MyD88/JNK信号通路的电针曲池、足三里穴治疗脑缺血再灌注损伤的作用机制

目的:探讨电针曲池、足三里穴是否通过TLR4/My D88/JNK信号通路产生脑缺血再灌注损伤的保护作用。方法:将36只SD大鼠随机分为假手术组、模型组及电针组,以大脑中动脉闭塞(MCAO)法建立大鼠局灶性脑缺血再灌注模型。采用TTC染色观察脑缺血后梗死体积;采用蛋白免疫印迹法观察缺血周边区脑组织中TLR4、My D88的蛋白表达以及JNK的磷酸化水平。结果:电针曲池、足三里穴可明显改善MCAO大鼠的神经功能缺损症状和脑梗死体积(P0.05);电针可以抑制缺血周边区脑组织中TL4、My D88的蛋白表达(P0.05),降低JNK的磷酸化水平(P0.05)。结论:电针曲池、足三里穴可能通过抑制TLR4/My D88信号通路,降低JNK的磷酸化,从而产生对脑损伤的神经保护作用。

The mechanism of electroacupuncture at Quchi and Zusanli acupoints on cerebral ischemia and reperfusion injury based on TLR4/MyD88

Abstract Objective: To investigate if the TLR4/MyD88/JNK signaling pathway mediates the protective effect on cerebral ischemia reperfusion injury by Electroacupuncture (EA) at Quchi, Zusanli. Method: The 36 SD rats were randomly divided into sham operation group, model group and EA group. The focal cerebral ischemia reperfusion model was established by middle cerebral artery occlusion (MCAO) in rats. TTC staining was used to observe the infarct volume after cerebral ischemia, and the expression of MyD88 and TLR4 in the ischemic surrounding region was observed by Western blotting. The phosphorylation level of JNK was observed by Western blotting. Result: EA at the Quchi and Zusanli acupoints could significantly improve the neurological symptoms and relieve the cerebral infarct volume in MCAO rats (P<0.05).EA could inhibit the expression of TLR4 and MyD88 protein in the ischemic surrounding region (P<0.05) and reduce the phosphorylation of JNK(P<0.05). Conclusion: EA at the Quchi and Zusanli acupoints exerts neuroprotection against the cerebral ischemia and reperfusion injury by reducing phosphorylation of JNK and inhibiting the TLR4/MyD88 signaling pathway.